VE-cadherin Double Nickase Plasmid (m2): sc-419596-NIC-2
- Target species: mouse
- 20 µg of transfection-ready, purified plasmid DNA; Suitable for up to 20 transfections
- VE-cadherin Double Nickase Plasmid (m2) consists of a pair of plasmids each encoding a D10A mutated Cas9 nuclease and a target-specific 20 nt guide RNA (gRNA) designed to knockout gene expression with greater specificity than its CRISPR/Cas9 KO counterpart
- Paired gRNA sequences are offset by approximately 20 bp to allow for specific Cas9-mediated double nicking of the genomic DNA, which mimics a DSB
- One plasmid in the pair contains a puromycin-resistance gene for selection; the other plasmid in the pair contains a GFP marker to visually confirm transfection
- VE-cadherin Double Nickase Plasmid (m2) and VE-cadherin Double Nickase Plasmid (m22) encode distinct paired gRNA designs targeting Cdh5. One or both designs may be available
- Following transfection, gene knockout efficiency can be assayed by WB, IF or IHC using antibody: VE-cadherin Antibody (F-8): sc-9989
Ordering Information
| Product Name | Catalog # | UNIT | Price | Qty | FAVORITES | |
VE-cadherin Double Nickase Plasmid (m2) | sc-419596-NIC-2 | 20 µg | $410.00 |
Mouse Cdh5 encodes VE-cadherin, an endothelial-specific adherens junction protein that mediates homophilic cell–cell adhesion to maintain vascular barrier integrity and vessel stability. VE-cadherin links to catenins and the actin cytoskeleton to coordinate junctional remodeling during angiogenesis and endothelial polarization, and it interfaces with VEGF/VEGFR2 and Rho-family GTPase signaling to regulate permeability and leukocyte transmigration. Dysregulated Cdh5/VE-cadherin function is implicated in pathological vascular leak, inflammation-associated endothelial dysfunction, and aberrant neovascularization observed in tumor microenvironments and retinopathies. Gene editing of mouse Cdh5 supports mechanistic studies in endothelial biology, including junction dynamics, angiogenic sprouting assays, and in vivo models of vascular development and barrier disruption.
VE-cadherin Double Nickase Plasmid (m2) consists of a matched pair of plasmids engineered for high-specificity editing of the Cdh5 locus in mouse cell lines. Each plasmid expresses a Cas9 D10A nickase and a distinct sgRNA targeting opposite DNA strands within Cdh5. When directed to adjacent sites on opposite DNA strands, the two nickases generate offset single-strand nicks that together produce a staggered double-strand break, requiring coordinated on-target activity from both guides. The resulting DNA break is resolved by endogenous cellular repair pathways, most commonly through non-homologous end joining (NHEJ), leading to insertions or deletions that disrupt Cdh5 function. By requiring dual sgRNA engagement at the target locus, the double nicking approach enhances editing specificity and provides a complementary CRISPR strategy for applications where additional control over targeting precision is desired.
To support efficient identification of edited cells, one plasmid encodes GFP for fluorescent visualization of transfected populations, while the companion plasmid carries a puromycin resistance gene for antibiotic selection. Together, these features support efficient enrichment of co-transfected populations and simplify the validation of Cdh5-disrupted clones.
For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.